This review focuses on the possible role of transforming growth factor-beta isoforms 1-3 (TGFbeta) in prostate cancer. TGFbeta1 appears to inhibit the cellular proliferation of normal prostate cells. Surprisingly, TGFbeta1 is overexpressed in prostate cancer. To help explain this apparent paradox, it has been revealed that with tumor progression, prostate cancer cells acquire reduced sensitivity to the growth-inhibitory effects of TGFbeta1. Aberrations of the TGFbeta1 signaling pathway at the prereceptor, receptor, or postreceptor level may lead to prostate cancer cell resistance to TGFbeta1 growth inhibition. Indirectly, elevated levels of TGFbeta1 may induce host effects that may be beneficial to prostate tumor growth by suppressing the immune system, promoting angiogenesis and extracellular matrix formation, and enhancing metastatic potential. Consequently, TGFbeta1 appears to be important in prostate carcinogenesis and tumorigenicity. TGFbeta2 and TGFbeta3 are only briefly presented as very little is known about their role in prostate cancer.